Epidemiological data suggest that regular exposure to passive heat, using methods such as sauna bathing and hot water immersion, is associated with a reduction in cardiovascular disease (CVD) risk. Reductions in CVD risk are also observed in those who regularly exercise, raising the possibility of shared physiological mechanisms. Given the well-documented inflammatory component of CVD, the role of inflammation in mediating the cardioprotective effects of passive heating hence warrants further investigation.

A single bout of exercise can induce an acute inflammatory response, which has been proposed as a mechanism explaining the long-term reduction of chronic low-grade inflammation seen with regular exercise. A similar mechanism may underlie the benefits of passive heating. Supporting this, blunting the increase in body temperature during exercise also attenuates the acute inflammatory response. Others showed that exposing isolated tissue to heat, without muscle contraction, can induce an inflammatory response. Whole-body exposure to heat induces an acute inflammatory response of a magnitude similar to low- to moderate-intensity exercise, and reductions in resting inflammatory markers have been documented in chronic passive heating studies. These findings imply that temperature itself, independent of muscle contraction, can modulate inflammation.

Further insights come from spinal cord injury models, which highlight the role of the sympathetic nervous system in inflammation. Adrenaline can independently induce an inflammatory response, but even in high-level spinal cord injury, which results in a blunted adrenaline response, passive heat exposure still triggers an inflammatory response. This, again, suggests an independent temperature-related mechanism, potentially mediated by heat shock elements. These have been suggested to help regulate the production of a key inflammatory marker, interleukin (IL)-6. The IL-6 response is primarily affected by core and muscle temperature, and not by alterations in skin temperature. This is relevant for the wider uptake of heat therapy, as locally cooling the skin, particularly the face, enhances thermal comfort and perceptions, potentially influencing adherence to long-term heat therapy protocols. Given that the sustainability of heat therapy is crucial for its potential health benefits, optimising perceptions of heat exposure may play a critical role in increasing its uptake.

Despite promising preliminary findings, the majority of passive heating studies have been conducted in acute settings in young and relatively healthy populations. However, the long-term effects, and the effects in other demographic groups, remain sparsely investigated. Given that inactive populations (e.g., those affected by pain, frailty, disability) often exhibit an elevated inflammatory profile, they may particularly benefit from heat therapy. Another practical shortcoming of some existing studies is the use of protocols of long duration (up to 2 hours) or intense heat stress (up to core temperatures of 39.5°C), raising questions about the feasibility of any implementation in a real-world setting.  To better understand the therapeutic potential and use of heat therapy as a non-exercise intervention for cardiovascular health, future research should therefore focus on developing tolerable, yet effective, protocols for those at higher risk for CVD.